Department of Pharmaco-Biology, University of Calabria, Rende, Cosenza, Italy.
J Bioenerg Biomembr. 2010 Aug;42(4):321-8. doi: 10.1007/s10863-010-9293-8. Epub 2010 May 21.
The effect of hypothyroidism, induced by 6-n-propyl-2-thiouracil (PTU) administration to rats, on the retinoylation reaction and oxidative status was investigated in rat-testes mitochondria. In hypothyroid mitochondria, when compared to euthyroid controls, we found a noticeable increase in the amount of all-trans-retinoic acid (atRA) bound to mitochondrial proteins by an acylation process (34.2 +/- 1.9 pmoles atRA/mg protein/360 min and 22.2 +/- 1.7 pmoles atRA/mg protein/360 min, respectively). This increase, which was time- and temperature-dependent, was accompanied by a strong reduction in the cardiolipin (CL) amount in the mitochondrial membranes of hypothyroid (2.6 +/- 0.2%) as compared to euthyroid rats (4.5 +/- 0.5%) Conversely, a decreased retinoylation reaction was observed when CL liposomes were added to mitochondria or mitoplasts from both euthyroid and hypothyroid rats, thus confirming a role of CL in the retinoylation process. In mitochondria from the latter animals an increase of the level of oxidized CL occurred. The ATP level, which was reduced in hypothyroid mitochondria (27.3 +/- 4.1 pmoles ATP/mg protein versus 67.1 +/- 8.3 pmoles ATP/mg protein of euthyroid animals), was surprisingly increased in mitochondria by the retinoylation reaction in the presence of 100 nM atRA (481.5 +/- 19.3 pmoles ATP/mg protein of hypothyroid animals versus 84.7 +/- 7.7 pmoles ATP/mg protein of euthyroid animals). Overall, in hypothyroid rat-testes mitochondria the increase in retinoylation activity correlates with a significant depletion of the CL level, due to a peroxidation of this lipid. In addition, an enhanced production of reactive oxygen species was observed.
甲状腺功能减退症,由 6-正丙基-2-硫代尿嘧啶 (PTU) 给予大鼠引起,对大鼠睾丸线粒体的视黄酰化反应和氧化状态的影响进行了研究。在甲状腺功能减退症的线粒体中,与甲状腺功能正常的对照组相比,我们发现通过酰化过程结合到线粒体蛋白上的全反式视黄酸 (atRA) 的量明显增加(34.2 ± 1.9 pmoles atRA/mg 蛋白/360 min 和 22.2 ± 1.7 pmoles atRA/mg 蛋白/360 min)。这种增加是时间和温度依赖性的,伴随着甲状腺功能减退症(2.6 ± 0.2%)的线粒体膜中心磷脂(CL)含量的强烈减少与甲状腺功能正常的大鼠(4.5 ± 0.5%)相比。相反,当 CL 脂质体被添加到来自甲状腺功能正常和甲状腺功能减退症大鼠的线粒体或线粒体膜时,观察到视黄酰化反应降低,从而证实了 CL 在视黄酰化过程中的作用。在后一种动物的线粒体中,氧化的 CL 水平增加。ATP 水平在甲状腺功能减退症的线粒体中降低(27.3 ± 4.1 pmoles ATP/mg 蛋白与甲状腺功能正常动物的 67.1 ± 8.3 pmoles ATP/mg 蛋白相比),但在存在 100 nM atRA 的情况下,线粒体中的视黄酰化反应出乎意料地增加(甲状腺功能减退症的 481.5 ± 19.3 pmoles ATP/mg 蛋白与甲状腺功能正常动物的 84.7 ± 7.7 pmoles ATP/mg 蛋白相比)。总体而言,在甲状腺功能减退症大鼠睾丸线粒体中,视黄酰化活性的增加与 CL 水平的显著耗竭相关,这是由于该脂质的过氧化。此外,观察到活性氧物质的产生增加。